Author: Yenis Paez-Perez

HPI: 35 yo otherwise healthy male presents to the Emergency Dept. (ED) with a laceration over the palmar surface of the left hand, proximal to the PIP joint and extending over the MCP joints of the 4th and 5th digit. He sustained this injury at work one hour ago. He is a firefighter and was responding to a house fire when he accidently tripped over an object in a smoke filled room while putting on his glove. He states his left hand went through a glass door. At the scene, patient washed it out with sterile saline and a dressing was applied. Pt also complaints of decreased sensation to the distal aspect of his left 5th digit. He denies any other trauma, preceding symptoms of chest pain, dizziness, feeling lightheaded, palpitations, inhalation injury or difficulty breathing. Denies head injury, neck pain or LOC. Last tetanus is unknown.

Physical Exam:

Vitals: BP 155/97 Pulse 97 RR 15 T 98.6F SpO2 100% on RAMSK/extremities: 2.5cm complex “V” shaped laceration over the palmar MCP of the left 5th digit that is oozing blood; no arterial bleeding noted. Tissue flap noted. 1.5 cm laceration over the left palmar aspect of the 4th digit between the MCP and PIP joint. Hemostasis noted. Small tissue flap noted. Sensation intact over the distal left 4th digit; Sensation mildly decreased over the distal left 5th digit. Cap refill brisk both digits. Pt is able to flex and extend both digits.

Digital block was performed on the 4th and 5th digits of the left hand by injecting lidocaine into the web spaces as well as local was performed on the palm where the digital block was ineffective.

Moderate bleeding/oozing noted of the 5th left finger laceration. Upon lifting the tissue flap of the 5th digit the flexor tendon was exposed but not lacerated. The 4th left digit wound more superficial. No tendon exposed. No FB found in either laceration.

For lacerations to the hand or other injuries that may or may not involve a tendon always ask:

Position of hand injury?

Crush, burn, injection, chemical injury?

Other trauma or preceding symptoms?

Exam for hand/wrist lacerations

Check and compare Bilateral grip strength

Check sensation

Compare bilaterally with 2 point discrimination to the volar aspect of each fingertip

Normal 2 point discrimination on the hand is 5-6 mm

Review of nerve distribution :

Check Motor function

Ask them to make a clenched fist— The middle and distal phalanges should all be parallel to each other with the nails positioned in the same plane and pointing toward the Scaphoid when fist is clenched

Ulnar Nerve innervates the Lumbricals and Adductor Pollices Muscles

Lumbricals: Have patient abduct their fingers and have them resist the force of you pushing their fingers back to midline

Adductor Pollices Test: Have patient hold a piece of paper with the volar pulp of the thumb and PIP of index finger. If you pull away at the paper, and pt is able to maintain the key pinch of paper against resistance then adductor pollicis is strong.

Opposition (Thenar Muscles): As them to touch their pinky with their thumb

Ask pt to abduct their thumb with palm up and have the pt resist a force to redirect the thumb toward the palm (Abductor Pollicis longus)

Radial Nerve

With palm on the table, hyperextend all fingers against resistance from can have them lay their palm flat on a table, and lift each digit straight up and extend up from the table while keeping the palm flat

Vascular

Check for capillary refill and pulses

Flexor Tendor Testing

90% of the tendon can be severed/lacerated with preservation of ROM without RESISTANCE.

Apply resistance when testing for tendon function

Pain along course of tendon during resistance testing suggest partial laceration even if pt has FULL ROM

Test for Flexor Digitalis Profundus (FDP): Ask the to flex their DIP joint against resistance while holding their MCP and PIP joint in extension

Test for Flexor Digitalis Superficialis (FDS): Ask to flex their PIP joint against resistance while ALL the rest of the fingers are held in full extension (Hyperextension disengages FDP and the FDS function is isolated).

Imaging

If isolated fingers involved, get a AP, oblique and lateral view of the designated finger as well as the hand

Digital Blocks

Web Space– Inject 1-3 mL of Anesthetic

Transthecal

Inject into flexor Tendon sheath

ID distal palmar crease and tendon

Insert needle at 45 degrees just distal to crease

Inject

If resistance, withdraw slightly

Apply proximal pressure

Pros: Only 1 poke and numbs entire finger

Cons: It’s over most sensitive part of the hand

Method to get a bloodless field

Use tourniquet or Penrose drain at base of finger secured by hemostat

Use another tourniquet or gauze to wrap around distal end of finger and wrap w/ moderate compression down from most distal part to laceration milking out the blood in the distal finger

HPI: 46-year-old female w/ PMH of asthma, SLE, RA and seizure disorder presents to the emergency department by BLS for evaluation. Patient states, “I don’t like people accusing me of doing things I didn’t do, I only took 2 Percocet and that’s it!” Patient states that she has been feeling depressed and “everything I do is never good enough for my kids, I buy them car, and I don’t even have car myself.” Patient appears to have multiple scratches over her face and left wrist, but is not willing to elaborate how she sustained them or provide any additional history. Denies any suicidal ideations, homicidal ideations, or hallucinations. There is no known psychiatric history.

Per family and EMS, patient was in her bedroom with the door shut, “not acting right, she was asking for us to pass her the key under the door to get out of the room but there is no lock on the door. She did this once before but it went away, today is more severe.” Pt was found in her bedroom by EMS with 2 empty beer cans and bottles of Percocet nearby. She had a recent URI for which she was taking Zzz-quil.

Working Diagnosis: Anion gap metabolic acidosis, most likely due to ethylene glycol poisoning

ED/Hospital course: In the ED patient became increasingly altered. Upon arrival patient was coherent, AAOx3, tearful. Upon reevaluation she was found in room shaking back and forth talking to herself and banging her hands on the bed rails, more confused, inappropriate in her thoughts and actions. A short time later she was found on the floor next to stretcher and was AAOx1, agitated, combative, not following commands, fighting with staff, incontinent of urine. Lab results returned at this time and the patient was subsequently intubated, received 1 amp sodium bicarbonate prior to intubation and admitted to MICU. Repeat labs in MICU showed persistent anion gap metabolic acidosis with Bicarbonate of 5 and anion gap of 26. She was placed on bicarbonate drip and received emergent HD. After HD, the acidosis improved with a bicarbonate value of 19 afterwards. Additionally placed on fomepizole. Received 2 rounds of HD. Subsequently extubated and transferred to floor. Upon extubation she continued to deny any SI or toxic ingestion. Methanol and ethylene glycol levels (-), however, they were drawn after HD was performed.

Positive birefringent calcium oxalate crystals in the urine; often absent initially commonly described as “envelope-shaped”

May see hypocalcemia although not always present

Management:

Alcohol dehydrogenase inhibitors: Fomepizole or ethanol

Hemodialysis with same indications as methanol above

Thiamine and pyridoxine can be administered to decrease production of oxalic acid

Isopropanol

Isopropyl (rubbing) alcohol

More intoxication/CNS depression but generally less severe sequlae than methanol and ethylene glycol 80% is absorbed from the stomach within 30 minutes and metabolized by alcohol dehydrogenase to acetone

Lactic acid on lab analysis may be falsely elevated and vary depending on how the sample is analyzed. You will note that ABG lactic acid and serum lactic acid analyzed by lab are very different values, this is due to the fact that a metabolite of ethylene glycol’s metabolism has a very similar chemical structure to lactic acid, causing a falsely positive elevated lactic acid

The differential diagnosis of anion gap metabolic acidosis listed above is a limited list of the most commonly noted causes of AG metabolic acidosis; a comprehensive list is much broader

An osmolar gap >50 is highly suggestive of toxic alcohol ingestion; a level >100 is virtually pathognomonic—there is really nothing else that can cause such a severely elevated osmolar gap other than toxic alcohol

Case presented by Dr. GregnCassidy

Special thanks to Dr. Kashani for his guidance in preparing this case.

Scavenger Hunt in Hoboken !

HPI: 7 day old female presents to the Emergency Dept. (ED) after being seen earlier in clinic. Mother is rom Nigeria and arrived to the U.S a few weeks prior to delivery. Prenatal care is unclear. Patient was delivered via C-Section at 39 weeks at another nearby hospital. Both mother and baby spent one day in the hospital after delivery being discharged home. Mother states that since last night, the baby appears to “ not breathing right.” She also hasn’t’ been eating much and is crying more often than usual, during which her lips start to turn blue.

ED/Hospital course: Patient was admitted to PICU, underwent Echocardiogram and further imaging and was diagnosed with Coarctation of the Aorta. The patient was transferred to Mt. Sinai for operative repair.

Pearls:

7 day olds are terrifying, especially if they are sick.

Take a breath! Start with your ABCs.

Coarctation of Aorta(CoA) is a congenital aortic narrowing which most commonly occurs at the level of ductus arteriosis. There are Pre-ductal and Post-ductal types. Pre-Ductal CoA is a Truncus dependent lesion and most patients present within 2 weeks of birth once duct closes. Aortic narrowing leads to increased LV function and dilation. Post-ductal are commonly identified in adulthood.

Obtain a BP/pulse Ox in all 4 extremities

Perform the Hyperoxia test

Obtain ABG on RA. Then, apply 100% supplemental oxygen with a NRB for 10-15 minutes. Repeat the ABG on the NRB.

You may also apply supplemental oxygen and assess the infant’s response. If saturation increases to at least 5-10%, it’s most likely a Lung problem. If it remains the same, think about Congenital Heart Disease

Prostaglandin (pt is less than 4 weeks old typically 1-2 weeks of life) start at 0.05 mcg/kg/min.

Dr. Hochman rule #11, call consultants early “don’t be the captain of a sinking ship”

3-year-old boy presents to the ED with a 4-day history of cough and 1-day history of fever. Per family patient has been having rigors and chills with vomiting. He also reports chest pain with coughing. His immunizations are UTD. The child does not appear toxic,

VS: Temp 103.3F, BP 90/65, HR 100, RR 30, 96% O2 Saturation on RA.
Patient has some intercostal retractions, with decreased air entry on the right side with audible crackles.

Questions for EM physician

How do you make the diagnosis of pneumonia?

Distinguishing patients with bacterial pneumonia, who would benefit from antibiotics, from those with nonbacterial pneumonia who would not.

Who requires inpatient management vs. patients that can be safely discharged home on oral antibiotics.

Pneumonia is the number 1 killer of children worldwide.

Pneumonia occurs more often in early childhood than at any other age and causes significant morbidity and mortality.

Identifying the cause of pneumonia in children is difficult due to a lack of rapid, accurate, commercially available laboratory tests for most pathogens. Empirical therapy based on patient’s age, clinical scenario and risk factor is the most common course in most cases.

Age-specific causes of pneumonia in otherwise healthy children. Pathogen listed in order of frequency

*Infants (1 – 3 months of age) may present with a characteristic syndrome of cough, tachypnea, progressive respiratory distress, and radiographic evidence of bilateral diffuse pulmonary infiltrates with air trapping. Most are afebrile. This syndrome is also called APS. The most common pathogen included Chlamydia trachomatis and respiratory viruses. Infection of Bordetella pertussis should also be considered due to recent dec. in immunization. Acutely, APS is generally benign and self-limiting disease. In such cases, infants often have viral illness, which does not respond to antibiotic therapy, but differentiating bacterial from viral illness is often difficult. Consider empiric antibiotic therapy.

Diagnosis of pneumonia:

Definition: Essentially it is infection of lower respiratory tract in the presence of radiographic abnormalities on CXR.

WHO guidelines for pneumonia in children is cough and tachypnea

Age < 2 months: Tachypnea is >60 RR

Age 2 months to 5 months: Tachypnea is >50 RR

Age >12 months: Tachypnea is > 40 RR

Clinical features

Fever and tachypnea are sensitive but not specific

Cough

Productive cough is rarely seen before late childhood

Consider pneumonia in any child presenting with prolonged fever, prolonged cough, high fever, as well as focal respiratory findings not including wheezing, especially with the presence of multiple symptoms.

HPI: 49-year-old female brought in via ALS presents complaining of Chest pain. As per the Paramedics, the patient was found to be in no acute distress, stating she had exertional chest pain, which had subsided. The pre-hospital ECG was suspicious for ischemia and she was given ASA. Patient states she was walking home from the store when she began to have a pressure like pain on the left side of her chest, which was non-radiating and persisted when she laid down. She admits to feeling similar symptoms over the past few months, but today was the most severe. Upon arrival to Emergency Department, she denied chest pain, SOB, palpitations, abdominal pain, nausea or vomiting. Denied ETOH or illicit drugs use

ED Course: Repeat ECG in ED showed NSR and had completely normalized. Case was discussed with Interventional cardiologist on call. A Code STEMI was activated and patient was taken emergently to the Cath lab. She was given a Heparin bolus as well as Plavix.

ED/Hospital course: The catheterization report revealed 80-90% Distal left main, 30 % mid LAD, and LM stenosis improved partially during catheterization with nitroglycerin. Patient admitted to recently using cocaine. CT surgery was called due to the fact that patient had recent cocaine use and it was believed she might have had Left Main Coronary spasm. On hospital day 2, patient went back for repeat catheterization, which revealed Left main distal 30% and LAD mid 30% stenosis. Patient was transferred to telemetry, and discharged on hospital day 4.

Pearls:

aVR in ACSTypical ECG findings with left main coronary artery (LMCA) occlusion:

(Don’t worry so much about STE 0.5mm or less in lead aVR, because it lacks specificity. Using 1.0mm or greater in lead aVR, has better specificity)

ST-Segment Elevation in lead aVR foreshadows a worse prognosis in ACS and often predicts the need for CABG. Patients with NSTEMI and ST elevation ≥ 1mm in aVR are likely to have multi-vessel or LMCA disease and are likely to require CABG, therefore withholding Clopidogrel may be prudent. ST-segment elevation in aVR can be caused by any of the following 4 mechanisms

Transmural infarction of the basal septum due to a very proximal LAD occlusion or complete LMCA occlusion (patient will be VERY sick)

Severe multi-vessel coronary artery disease.

Diffuse sub-endocardial ischemia from oxygen supply/demand mismatch.

Patients with complete occlusion of the LMCA (mechanism 2), often present in cardiogenic shock and require immediate revascularization. Patients with acute coronary occlusions typically will have active symptoms and look sick!

There is an estimated 70% mortality without immediate PCI. Medical therapy (including thrombolytic) does not improve mortality. Emergency PCI may decrease mortality to 40%.

What Else can Cause STE in aVR that Won’t Benefit from Going to the Cath Lab?

HPI: 52 year old male with PMH of IDDM presents to the Emergency Dept. (ED) with left leg pain for the past 9 days which has become progressively worse. He is a taxi driver and reports that a part of the seat, which supports his legs, has been rubbing against his left hip/buttock/thigh and he thinks this is what’s causing the pain. He reports pain to the back of his left buttock, which radiates down the leg “like a shooting pain.” The patient has been to the ED multiple times already for similar complaints, requesting for stronger pain medications. He is upset because he feels the medicine just isn’t working. At this point, the patient is uncooperative and refuses to answer any more questions. Further history was obtained from his previous visit history, which stated he was discharged yesterday with a diagnosis of sciatica and a prescription for Lidoderm patch, Motrin and Percocet.

ED/Hospital course: Orthopedic Surgery was consulted. X-Ray did not show obvious bony involvement and ESR/CRP was not suggestive of osteomyelitis. MRI was performed on the LLE, which sowed a hyper-intense signal within multiple muscles of the pelvis and left thigh consistent with myositis. Collection within the Obturator Externus and Gluteus Maximus muscles likely represented an abscess consistent with pyomyositis. The patient was started on Vancomycin and Zosyn and sent to Interventional Radiology for drainage of the abscess. The cultures grew back MSSA. The left knee tap did not grow any organisms on Gram Stain. IR drainage was followed by orthopedic washout and debridement of the musculature with insertion of JP drain for continuous drainage. The patient’s antibiotics were switched to Levaquin and he was subsequently discharged home with Clindamycin and Bactrim for 2 more weeks. He tested negative for HIV.

Pearls & Takeaways:

Don’t blow off patient’s complaints! Our patient presented with History and Physical exam consistent with sciatica with a positive straight leg test. He was on Percocet and kept asking for stronger medications for his previously diagnosed Sciatica.

Make sure to undress the patient and examine the skin!

If the patient is complaining of pain out of proportion to his/her exam, dig a little deeper for alternative differential!

Since his Accucheck was High, further laboratory testing was done which revealed leukocytosis. The elevated white count prompted me to perform a further work up

Always re-evaluate the patient! On re-evaluation, he appeared sicker and with cool, damp skin on his back and neck, solidifying my gestalt that maybe I am missing something

Pyomyositis is a purulent infection of skeletal muscle that arises from hematogenous spread, usually with abscess formation.

Risk Factors: immunodeficiency (HIV).

auerus is the most common cause of pyomyositis; it causes up to 75 – 90% of cases.

Pyomyositis presents with fever and pain and cramping localized to a single muscle group. It develops most often in the lower extremity (sites include the thigh, calf and gluteal muscles) but any group of muscles can be involved including iliopsoas, pelvic, trunk, Paraspinal and upper extremities.

MRI is the most useful imaging modality for diagnosing the disease. It can distinguish the defining sites of infection and rule out other entities.

Nonspecific lab findings include Leukocytosis and elevated inflammatory markers but CPK are often normal.

Empiric antibiotics should be directed against Staph/Strep for immunocompetent. Immunocompromised should be covered for Gram negative, gram positive and anaerobic organisms should be considered.

Pyomyositis is graded based on stages.

Stage 1 (Invasive stage, 1-2 weeks, may only have pain) can be treated with Antibiotics alone.

Most patients present with Stage 2 (Suppurative stage, weeks 3-4)

Stage 3 (Late stage) due to delay in diagnosis and usually requires drainage for definitive management.

HPI: 10 year old male with no significant past medical history presents to the Emergency Dept. complaining of painless vision loss in the right eye for 2-3 months. Patient states he has been having difficulty seeing out of his right eye for 2 months despite changing positions in class, taking on and off his glasses and using eye drops. Vision loss has become progressively worse and now he can only distinguish whether lights are on or off. Mother states she did not do anything about this problem because she thought he was kidding and she didn’t’ have money or health insurance to seek medical attention. Patient has been wearing Bifocals for myopia since the age of 6, with corrective vision lenses at age 5. Denies associated trauma. Patient moved to the U.S from Nigeria 5 years ago. He lives with his mother and sister. Vaccines are up to date.

PMH/Birth History: NSVD at 39 weeks, 1 day. Birth took place in Nigeria and mother denies any infection during or after pregnancy. Following birth, patient did not have any complications such as pneumonia, eye infections or rashes.

Social History: Denies drug abuse. Denies exposure to chemicals. Denies contact with dirt, dogs or pigs. Patient did not live on a farm. As per mother, there was no domestic abuse in the family

PHYSICAL EXAM

Vitals within normal Limits

General: In no acute distress, appears stated age.

Head: Atraumatic, normocephalic. No deformities.

Eye: Right (OD): pupil non-reactive and remains white in color and approximately 2mm. Afferent reflex is present CN II; efferent reflex is absent. There is a complete visual field defect on the right side. Visual Acuity: Can only distinguish between light and dark. Unable to count fingers at any distance or visual objects even in motion. On Fundoscopic exam, the fundus is gray/dull, with no retina visualized. ALL CONSISTENT WITH LEUKOCORIA

Bedside U/S: Completed within 10 minutes of arrival ( Only Right eye is shown)

Working Differential Diagnosis:

Retinoblastoma

Intraocular Mass

Cataract

Syphilis

Parasitic infiltrate

Posterior Infarct

CT Max/Facial w/o Contrast to rule out intracranial pathologies: Negative for masses; positive for homologous material in the right lobe. MRI was recommended for further evaluation

ED/Hospital course: Ophthalmologist on call was consulted, and said there was nothing more to do. Unfortunately because his vision loss was > 2 months, no life saving surgery was imminent as the retina was already detached causing ischemia to the rods and cones within it. Patient was to follow up in ophthalmology clinic the following day. Patient’s Pediatrician was also contacted and he referred the patient to a Pediatric Ophthalmic specialist in University Hospital, with a scheduled appointment within the same week. Approximately one week ago, patient underwent surgery and the leading diagnosis was Toxocariasis as per MRI. Biopsy results to follow. As per mother, the patient is still without vision in his right eye.

LEUKOCORIA, UNILATERAL, 10 YO MALE DIFFERENTIALS

Coats disease— is an exudative retinal vascular disorder characterized by retinal telangiectasias and subretinal exudation leading to serous retinal detachment. Presenting complaints include decreased visual acuity, strabismus, or leukocoria. The leukocoria in Coats disease is generally more yellow than white due to the presence of subretinal lipid. Coats disease is almost always unilateral and the vast majority of cases occur in boys. The majority of cases presenting with leukocoria are diagnosed between five and nine years of age, which is older than the majority of retinoblastoma patients.

Clinical examination: subretinal lipid and abnormal telangiectatic vessels US: demonstrates complete retinal detachment with massive subretinal lipid. Intraocular calcification is almost never present in Coats disease, another feature that helps to distinguish it from retinoblastoma.

The retinal photograph depicts bullous retinal detachment in the Left eye of a 1-year-old child with Coat’s disease simulating retinoblastoma. The magnetic resonance images confirm the diagnosis of retinal detachment and exclude retinoblastoma because of the absence of intraocular mass.

Toxocariasis — Toxocariasis, or visceral larva migrans, is an infection caused by the dog ascarid Toxocara canis or, less commonly, the cat ascarid Toxocara catis. There may be a history of living in an underdeveloped country, and exposure to dirt or undomesticated dogs. It occurs most commonly in children one to five years of age. Common presenting signs of toxocariasis are strabismus and poor vision. The ocular lesion is caused by the inflammatory response to the second-stage larva, which may localize in the one eye or both eyes

Chorioretinitis characteristic of toxoplasmosis. A pigmented scar is seen with an adjacent area of active chorioretinitis. The diagnosis of toxoplasmosis is based primarily on the appearance of the chorioretinal lesion rather than serologic studies. Courtesy of James T Rosenbaum, MD.

Retinopathy of prematurity (ROP) — developmental vascular proliferative disorder that occurs in the incompletely vascularized retina of preterm infants and can lead to retinal detachment and permanent blindness. The most important risk factor for developing ROP is prematurity. There needs to be a history of prematurity, and/or mother mentions patient was on O2 for awhile.

Vitreous hemorrhage — Vitreous hemorrhage causes leukocoria when there is extensive organization of the blood into a clot before degradation. With time, the reddish hue of the blood is lost and the hemorrhage transforms into “whitish debris.” Etiology includes advanced ROP, trauma (MOST common), leukemia or hemorrhagic disease of newborn

Retinablastoma– Retinoblastoma is the most common primary intraocular malignancy of childhood and accounts for 10 to 15 percent of cancers that occur within the first year of life. Retinoblastoma typically presents as leukocoria in a child under the age of two years. Untreated retinoblastoma is a deadly disease; however, with advances in treatment, survival in the contemporary era is >95 percent. Most common age group is birth- 2 years. Very uncommon in children over the age of 5, although 1-2 case reports have occurred in 18 year old males

Pearls & Takeaways:

Leukocoria Requires further investigation – On exam, History and Diagnostic

The use of tonometry, fundoscopy and ocular ultrasound are an easy, noninvasive way to add to your ophthalmic exam. Slit-lamp exam could have been considered here

Ocular ultrasound is really cool and fun!

Advocate for your patients! Make sure they have proper follow up with a specialist

If any abuse or neglect is suspected, be sure to turn on “Sherlock Holmes” senses and investigate.

Upper Abdominal U/S: Normal Liver and spleen. The spleen measured 10.9 cm in greatest dimension and was homogeneous in echotexture. No focal splenic lesion identified. The liver measured 16.5 cm and appeared normal.

EKG:

Working Diagnosis:

Thrombotic Thrombocytopenia Purpura (TTP)

Idiopathic Thrombocytopenic Purpura (ITP)

Hemolytic Uremic Syndrome (HUS)

Anemia due to blood loss

Infection/Sepsis

ED Course: On further questioning, patient states she has been menstruating for 3 weeks now and bleeding is heavier as compared to the previous cycle. In the ED, patient was given NS 0.9% 1000mL IV bolus once, Zofran 4 mg IV once, Reglan 10mg IV once. Type and screen and blood cultures were also sent and patient was admitted to the Medical ICU for thrombocytopenia and anemia.

Hospital Course:

In the Medical ICU, further lab results demonstrated elevated the following:

LDH: 699 Fibrinogen: 410 Haptoglobin: < 10 Troponin 0.44

Blood Cultures: No Growth

Urine Toxicology: Positive for cannabinoids

Hepatitis C antibody: < 0.1

HIV Ag/Ab: Non reactive

In the ICU, patient was given a 125mg bolus of IV Solu-Medrol and then started on 60mg IV every 8 hours. She was transfused 1 Unit of platelet with no response, as the following day, platelets actually dropped to 5.Hematology/Oncology was also consulted. They stated that the occasional schistocytes seen on blood smear with low Haptoglobin levels and elevated reticulocyte count and LDH was suggestive of microangiopathic hemolytic anemia, making TTP a more likely diagnosis. Heme/Onc recommended against any further platelet transfusion and ADAMS 13 levels were sent. On hospital day #3, patient’s LDH levels had increased to 1586 and Troponin was elevated to 1.2 with symptoms of dyspnea. Patient also had worsening anemia as hemoglobin dropped to 7.0, and platelets remained at 9. The same day, Surgery was consulted and patient was transfused 2 Units of PRBs and 2 Units of FFP in preparation for Shiley Catheter insertion for plasmapheresis. Cardiology was also consulted for the elevated troponin, which they attributed to ongoing demand ischemia without any evidence of ACS. Unfortunately, the following night at 1:25 AM and before a Shiley was ever placed, the patient became minimally responsive and Saturating at 90% on RA. Immediately, she became bradycardic and lost pulses. CPR was initiated as patient was simultaneously intubated. Total duration of CPR was 60 minutes. The patient received Epinephrine x 20, Amiodarone 300 mg x 1 and Insulin with 1 amp of D50W, Calcium chloride and Sodium Bicarbonate for Potassium of 6.1 on ABG. Sadly, the patient was pronounced at 2:25AM.

PEARLS : Thrombotic Thrombocytopenic Purpura (TTP)

PENTAD = ‘FAT RN”

Fever (50%)

Uncommon if they present early in the disease

High fever and chills suggest sepsis, so look for a source of infection.

Thrombocytopenia

MAJOR diagnostic criterion

Mean platelet of 25, 000 but they reach 5000.

Microangiopathic Hemolytic Anemia

MAJOR diagnostic criterion

Non-immune hemolysis with schistocytes

Results in elevated LDH, Low haptoglobin and high indirect bilirubin

Severely elevated LDH has been associated with MI, arrhythmias, shock and heart failure.

Menu

Disclaimer: Information contained on this website is the opinion of the authors and does not represent the opinion of St. Joseph's Regional Medical Center or St. Joseph's Regional Medical Center Emergency Medicine Residency Program.